Clinical and genetic studies focusing on the immune systems have highlighted the pivotal roles of inflammatory cytokines, such as interleukin (IL)-17, IL-23, and tumor-necrosis factor-α (TNF-α), and two fundamentally different cell types, including epidermal keratinocytes and mononuclear leukocytes, in the pathogenesis of psoriasis [1,4,5]. Here, TNF is linked to psoriasis.